Assuming you have the whole chromosomes genetic sequences (or long reads spanning the crossover breakpoints) yes, due to crossover with occurs during the making of gametes. So in the son there will be one of the two chromosome N (take N=2 if no crossover occured in chromosome 1..) that will be a mix of the mother's two copies of chromosome N.

On the other hand none of the mother's chromosome N will be a mix of the two copies of the son's chromosome N.

Can't we argue that by definition a live virus should have a reproduction number strictly greater than 1 (ie. exponential) and be able to spread from cells to cells? For PERV-A seems they obtain exponential replication in human 293T cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950858/figure/pone-0013203-g001/

All the translation (making of proteins) is done by the cell's ribosomes (this for almost every viruses) from mRNA strands as the cells do everydays to make proteins.

But the replication and transcription (making copies of the full length RNA genome and some mRNA copied from parts of it) is achieved by a viral polymerase, a RdRp.

This is for RNA viruses. Many DNA viruses do something along the same lines, but some do not and make their genome enter the cell nucleus to exploit either its DNA replication machinery or its DNA->RNA transcription machinery, or both.

Retroviruses are some kind of hybrid between the two strategies.

For coronaviruses the genome is translated into a big polyprotein which is cleaved in a dozen of proteins by a protease it includes. That dozen of proteins somehow self assemble into a replication complex which also makes the (lipid) ER membrane bubble. Into such a bubble the viral polymerase of the replication complex replicates the genome many times and also makes many subgenomic mRNA coding for the structural proteins. Eventually the bubble bursts and frees the many copies of the genome and the many subgenomic mRNA, those are translated and flood the environment with viral structural proteins. Together with the copied genomes all this mess self assemble into new virions. Both the bubbling and the natural cellular transport of membrane anchored proteins help the new virions to egress the cell.

Hope this helps your understanding of the standard strategy for virus replication.

See https://en.wikipedia.org/wiki/Sex-determining_region_Y_protein and https://en.wikipedia.org/wiki/Y_chromosome#Human_Y_chromosome

Most genes involved in male sexual characters are on other chromosomes but require a cascade initiated by expression of SRY (thus presence of Y chromosome) to be (un)expressed

Basic trignometry gives the irradiance curve, assuming that each region of the planet surface is disconnected from others (ie. no heat equation between day and night parts of the planet and whatever dominates its core temperature) and is at thermal equilibrium you can approximate the temperature with a constant time the 1/4th power of the irradiance

https://en.wikipedia.org/wiki/Stefan%E2%80%93Boltzmann_law

Obliquity is very low. The irradiance is proportional to the squared distance, that means that the irradiance oscillates between x and 0.43 x depending on the season.

This is roughly equivalent to the seasonal irradiance oscillation that you'll have on earth at 45° latitude north.

But as PlaidBastard said this computation is meaningless, as the very slow rotation on Mercury makes the day vs night dominate the seasons.

The water is moving due to gravity and it is braked due to frictional forces, with the land roughness at the bottom of the water column and with other water molecules at the top. Not hard to guess in what direction those two frictional terms are modified during a flood.

Search for https://www.ncbi.nlm.nih.gov/nuccore/?term=Ebolavirus%5Borganism%5D+AND+bat on genbank you'll find two batches of bat ebolavirus sequences: one 2019 paper https://pubmed.ncbi.nlm.nih.gov/31002301/ sequencing full Bombali ebolavirus genomes from bats, this study is considered trustful and indicates a bat origin of Bombali. This is also confirmed independently by some Predict sequences such as https://www.ncbi.nlm.nih.gov/nuccore/MT929359.1

And another 2005 paper https://www.nature.com/articles/438575a using nested PCR to obtain short partial Zaire ebolavirus (the genuine Ebola) sequences. This hasn't been replicated since 2005, this paper is not considered trustful.

There is a similar nested PCR story for Reston ebolavirus https://virologyj.biomedcentral.com/articles/10.1186/s12985-015-0331-3 but they didn't bother to upload the sequence to genbank..

Still Marburg (a distant filovirus) also has a clear bat origin.

Together with the serological studies and the lack of other putative reservoir it means that fruit bats are still our best guess.

But the truth is that we don't know for sure.

You can (estimate the) date the nodes of a tree and find in which branch the mutation appeared, thus estimating when it occurred.

H1N1 1918 was pretty severe and deadly in population lacking immunity. Yeah not much reason to assume that a H5N1 epidemic should be worse and that making a vaccine should be more difficult. Efficacy of H1N1 vaccines are hindered by the fact that we are all already immunized. In naive mice H1N1 and H5N1 are comparable.

In the simplest model there are 3 kind of mutations: neutral, positive, negative.

The rate at which neutral mutations accumulate (which really means the number of neutral mutations you'll observe between you and your parent) is roughly constant.

But the rate at which positive and negative mutations accumulate depend a lot on: how positive and negative they are (obviously mutations killing the organism won't accumulate) and how many they are among the total number of possible mutations.

When taking a bacteria adapted to a temperature of 20°C and putting it at 30°C the positive mutations (positive for this new environment) will accumulate very fast, at the beginning, and once the bacteria will be adapted to the new temperature there will be much less possible positive mutations, so their accumulation rate will slow down a lot.

Darwin's book is about inheritance as a broad concept, and the whole point of the book is to refine it a lot and use it to explain the evolution of species.

Go on https://timetree.org/ type Felidae in "build a timetree, Specify a Group of Taxa " then choose species and see the (time-scaled, ie. age of common ancestors) tree you get

You'll find 5 other Felis species with MRCA from 1.5 to 6 million years. Adding the few Prionailurus species with MRCA 9 million years you'll get something roughly equivalent to the Homo-Pan lineage in term of evolutionary history.

The Felis species really look like cats and the Prionailurus species are a bit wilder but still cattish, need to go farther to find something more like a Lynx or a Panthera (MRCA 12 million years so similar to the Apes lineage);